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Chronic hepatitis introduction

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Asmaa Eisa
Asmaa Eisa

Chronic hepatitis is characterized by a persistent inflammatory process in the liver lasting over 6 months. It is classified into three types based on histological features: chronic active hepatitis marked by necrosis and fibrosis carrying the worst prognosis; chronic persistent hepatitis with portal inflammation but no significant necrosis; and chronic lobular hepatitis involving hepatocyte apoptosis. Chronic hepatitis can be caused by viruses, metabolic disorders, drugs, or autoimmune conditions. Patients may be asymptomatic or experience fatigue, abdominal pain, jaundice, or liver abnormalities. Liver biopsy examines inflammation grade and fibrosis stage and helps establish etiology through immunological testing.

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Chronic hepatitis introduction
Definition Chronic hepatitis indicates a persistent, and often progressive, necroinflammatory process of the liver lasting more than 6 months and is characterized histologically by lymphocytic infiltration of the portal tracts together with varying degrees of parenchymal inflammation, hepatocellular injury, and fibrosis.
chronic hepatitis has been divided on morphologic grounds into three groups chronic active hepatitis Chronic hepatitis with piecemeal (periportal) necrosis (or interface hepatitis) with or without fibrosis. chronic persistent hepatitis chronic hepatitis with no significant periportal necrosis or regeneration with a fairly dense mononuclear portal infiltrate chronic lobular hepatitis chronic hepatitis with persistent parenchymal focal hepatocyte necrosis (apoptosis) with mononuclear sinusoidal infiltrates.
discrimination by differences in prognosis. uncomplicated portal inflammation and pronounced lobular inflammation respectively, were considered benign, nonprogressive lesions aggressive hepatocellular necrosis and fibrosis, was regarded as a serious, progressive process leading to cirrhosis
CAUSES Viruses Fatty infiltration inherited metabolic disorders Alpha 1-antitrypsin deficiency Alcohol autoimmune disease reactions to medications
Symptoms Asymptomatic or have only minor complaints The most common symptoms include The disease may have an insidious onset or may present abruptly; occasionally it follows an episode of acute hepatitis that fails to remit others exhibit features of chronic liver disease or hepatic failure fatigue or malaise, with mild abdominal discomfort, jaundice, anorexia, fever, nausea, or arthralgias
Extrahepatic manifestations amenorrhea, acne, gynecomastia, or Cushinoid changes Physical examination findings hepatomegaly, mild splenomegaly, and, occasionally, spider angiomas or palmar erythema Unfortunately, the clinical findings are not specific and correlate poorly with the severity of the disease.
The characteristic laboratory abnormalities include increase, usually of two- to 10-fold, in serum transaminase levels Other liver tests are generally normal or only mildly abnormal; increasing serum bilirubin, falling albumin levels, and a prolonged prothrombin time signal advanced, progressive disease Liver biopsy assessment in chronic hepatitis liver biopsy provides the best information available concerning the amount of hepatic fibrosis and the amount of ongoing inflammation and necrosis
Inflammation (Grade) Lobular Inflammation and Necrosis Grade Description Piecemeal Necrosis 0 No activity None None 1 Minimal Minimal, patchy Minimal; occasional spotty necrosis 2 Mild Mild; involving Mild; little some or all portal hepatocellular tracts damage 3 Moderate Moderate; involving all portal tracts 4 Severe Severe; may have Severe, with bridging fibrosis prominent diffuse hepatocellular damage Moderate; with noticeable hepatocellular damage
Degree of fibrosis (Stage) Stage 0: no fibrosis Stage 1: enlarged fibrotic portal tracts Stage 2: periportal fibrosis or portal to portal septa, without architectural distortion Stage 3: bridging fibrosis with architectural distortion, no obvious cirrhosis Stage 4: cirrhosis (probable or definite)
The etiology is established through Suggestive Histologic Findings Liver Immunohistochemistry HBsAg, HBeAg, HBV-DNA, HBcAg in liver Hepatitis B Ground-glass cells Hepatitis C Fatty change, Sinusoidal none inflammation, Lymphoid follicles, Bile duct damage Anti-HCV, Clinical history Hepatitis D none HDV antigen Anti-HDV, HDV-RNA, HDV antigen in serum or liver AutoimmuneAssociated none none Autoantibodies, Serum immunoglobulins Drug-Induced none none Drug history Copper accumulation, Fatty change, Glycogenated nuclei none Serum ceruloplasmin, Quantitative copper studies Wilson's Disease Alpha-1-Antitrypsin Deficiency HBsAg, HBcAg Definitive Diagnosis PAS-positive cytoplasmic globules Alpha-1-antitrypsin Serum levels and phenotyping
prognosis
Chronic hepatitis introduction

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Chronic hepatitis introduction

  • 2. Definition Chronic hepatitis indicates a persistent, and often progressive, necroinflammatory process of the liver lasting more than 6 months and is characterized histologically by lymphocytic infiltration of the portal tracts together with varying degrees of parenchymal inflammation, hepatocellular injury, and fibrosis.
  • 3. chronic hepatitis has been divided on morphologic grounds into three groups chronic active hepatitis Chronic hepatitis with piecemeal (periportal) necrosis (or interface hepatitis) with or without fibrosis. chronic persistent hepatitis chronic hepatitis with no significant periportal necrosis or regeneration with a fairly dense mononuclear portal infiltrate chronic lobular hepatitis chronic hepatitis with persistent parenchymal focal hepatocyte necrosis (apoptosis) with mononuclear sinusoidal infiltrates.
  • 4. discrimination by differences in prognosis. uncomplicated portal inflammation and pronounced lobular inflammation respectively, were considered benign, nonprogressive lesions aggressive hepatocellular necrosis and fibrosis, was regarded as a serious, progressive process leading to cirrhosis
  • 5. CAUSES Viruses Fatty infiltration inherited metabolic disorders Alpha 1-antitrypsin deficiency Alcohol autoimmune disease reactions to medications
  • 6. Symptoms Asymptomatic or have only minor complaints The most common symptoms include The disease may have an insidious onset or may present abruptly; occasionally it follows an episode of acute hepatitis that fails to remit others exhibit features of chronic liver disease or hepatic failure fatigue or malaise, with mild abdominal discomfort, jaundice, anorexia, fever, nausea, or arthralgias
  • 7. Extrahepatic manifestations amenorrhea, acne, gynecomastia, or Cushinoid changes Physical examination findings hepatomegaly, mild splenomegaly, and, occasionally, spider angiomas or palmar erythema Unfortunately, the clinical findings are not specific and correlate poorly with the severity of the disease.
  • 8. The characteristic laboratory abnormalities include increase, usually of two- to 10-fold, in serum transaminase levels Other liver tests are generally normal or only mildly abnormal; increasing serum bilirubin, falling albumin levels, and a prolonged prothrombin time signal advanced, progressive disease Liver biopsy assessment in chronic hepatitis liver biopsy provides the best information available concerning the amount of hepatic fibrosis and the amount of ongoing inflammation and necrosis
  • 9. Inflammation (Grade) Lobular Inflammation and Necrosis Grade Description Piecemeal Necrosis 0 No activity None None 1 Minimal Minimal, patchy Minimal; occasional spotty necrosis 2 Mild Mild; involving Mild; little some or all portal hepatocellular tracts damage 3 Moderate Moderate; involving all portal tracts 4 Severe Severe; may have Severe, with bridging fibrosis prominent diffuse hepatocellular damage Moderate; with noticeable hepatocellular damage
  • 10. Degree of fibrosis (Stage) Stage 0: no fibrosis Stage 1: enlarged fibrotic portal tracts Stage 2: periportal fibrosis or portal to portal septa, without architectural distortion Stage 3: bridging fibrosis with architectural distortion, no obvious cirrhosis Stage 4: cirrhosis (probable or definite)
  • 11. The etiology is established through Suggestive Histologic Findings Liver Immunohistochemistry HBsAg, HBeAg, HBV-DNA, HBcAg in liver Hepatitis B Ground-glass cells Hepatitis C Fatty change, Sinusoidal none inflammation, Lymphoid follicles, Bile duct damage Anti-HCV, Clinical history Hepatitis D none HDV antigen Anti-HDV, HDV-RNA, HDV antigen in serum or liver AutoimmuneAssociated none none Autoantibodies, Serum immunoglobulins Drug-Induced none none Drug history Copper accumulation, Fatty change, Glycogenated nuclei none Serum ceruloplasmin, Quantitative copper studies Wilson's Disease Alpha-1-Antitrypsin Deficiency HBsAg, HBcAg Definitive Diagnosis PAS-positive cytoplasmic globules Alpha-1-antitrypsin Serum levels and phenotyping